• β-1,3- d-glucan ;
  • cytokine release;
  • individual susceptibility;
  • lipopolysaccharide;
  • nasal challenge;
  • recycling workers;
  • whole blood assay


The aim of this study was to assess the cytokine response after nasal exposure to organic dusts.

In a double blinded, crossover study five garbage workers with occupational airway symptoms and five healthy garbage workers were intranasally exposed to endotoxin (lipopolysaccharide LPS), β-1,3- d-glucan (GLU), Aspergillus sp., compost or the saline dilute for 15 min. Nasal cavity volume and nasal lavage (NAL) were performed at baseline and 3, 6, 11 h postexposure. NAL was analysed with differential cell counts, cysteinyl-leukotrienes, tumour necrosis factor α, interleukin (IL)-1β, IL-6 and IL-8. A whole blood assay on cytokine-release was performed with LPS and GLU.

NAL cytokines neutrophils, lymphocytes and albumin increased significantly at 6 h after LPS exposure. GLU induced an increase in albumin and a slight increase in IL-1β 6–11 h post exposure. In the WBA a significant increase in all cytokines after exposure to LPS as well as GLU was found. Significantly more cells were seen in NAL of the control group 6 h post LPS exposure.

In conclusion lipopolysaccharide is the most potent inducer of inflammation in the nasal mucosa whereas compost and β-1,3- d-glucan only induce minor changes. This reaction to lipopolysaccharide is attenuated in workers with occupational airway symptoms. In whole blood assay, however, β-1,3- d-glucan also induces cytokine release, indicating a different protective effect of the nasal mucosa towards lipopolysaccharide and β-1,3- d-glucan.